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The α-diimine-type platinum(II) complexes having bulky perfluorinated phenyl groups were prepared and the molecular and crystal structures were revealed by X-ray analysis. They showed phosphorescence and electron-accepting properties. The organic light-emitting diode (OLED) devices showing green luminescence were fabricated.

BackgroundEMT has been proposed to be a crucial early event in cancer metastasis. EMT is rigidly regulated by the action of several EMT-core transcription factors, particularly ZEB1. We previously revealed an unusual role of ZEB1 in the S100A8/A9-mediated metastasis in breast cancer cells that expressed ZEB1 at a significant level and showed that the ZEB1 was activated on the MCAM-downstream pathway upon S100A8/A9 binding. ZEB1 is well known to require Zn2+ for its activation based on the presence of several Zn-finger motifs in the transcription factor. However, how Zn2+-binding works on the pleiotropic role of ZEB1 through cancer progression has not been fully elucidated.MethodsWe established the engineered cells, MDA-MB-231 MutZEB1 (MDA-MutZEB1), that stably express MutZEB1 (ΔZn). The cells were then evaluated in vitro for their invasion activities. Finally, an RNA-Seq analysis was performed to compare the gene alteration profiles of the established cells comprehensively.ResultsMDA-MutZEB1 showed a significant loss of the EMT, ultimately stalling the invasion. Inclusive analysis of the transcription changes after the expression of MutZEB1 (ΔZn) in MDA-MB-231 cells revealed the significant downregulation of LOX family genes, which are known to play a critical role in cancer metastasis. We found that LOXL1 and LOXL4 remarkably enhanced cancer invasiveness among the LOX family genes with altered expression.ConclusionsThese findings indicate that ZEB1 potentiates Zn2+-mediated transcription of plural EMT-relevant factors, including LOXL1 and LOXL4, whose upregulation plays a critical role in the invasive dissemination of breast cancer cells.

Many different quadrupedal walking patterns (gaits), such as walking , trotting , bounding and galloping can be generated by systems of coupled central pattern generators (CPG). However, the physiological mechanisms for the walking patterns are unclear. As a result, from an engineering viewpoint, many different mathematical models have been proposed to describe these walking patterns. In this report, we propose a hard-wired CPG network based on Rybak s model that can reproduce quadrupedal locomotion walking patterns. In this network, we use the beating model proposed by Hoshimiya et al. and the bursting model proposed by Maeda and Makino. The main purpose of this study was to reproduce the typical walking patterns; walking and bounding , with a hardware model, and to switch between these patterns using only one parameter, which can be interpreted as voltage stimulation from the midbrain locomotor region. We found the transition from the walking to the bounding behavior to be due to a relative weakening of the coupling between the CPGs in the network by stimulation from the midbrain locomotor region.